I'm in total agreement with Owen that V-K can reduce blood vessel calcification. However the downside is this gentleman also has A-fib. As such V-K can promote clotting factors which with A-Fib can and will cause clots to form which could have some bad effects. Promoting the clotting factors would be counter productive at this point.
Thought the discussion of vitamin K and AFIB merited its own discussion. Ergo, rather than detract from the thread on supplements for reducing high blood pressure, here we go.
I have always wondered about this standard medical advice (to avoid vitamin K) given to heart patients. The late Mr. Till was advised not to eat salads for this very reason!! (Which made some sense, I supposed, since he was on coumadin.) So heart patients are told to avoid vitamin K, yet their intestinal flora, if healthy, is making vitamin K 24/7 !?
I don't think vitamin K "promotes" clotting factors any more than vitamin C "promotes" collagen. In other words, taking enormous amounts of vitamin C does not create large callouses of collagen under the skin! The body makes what it needs, and then uses ascorbate for other purposes. I believe it is the same with vitamin K. I don't know of any evidence that the more vitamin K one takes, the more the blood tends to clot without any reason.
Yes, vitamin K is required in a clotting pathway, such that if it is not present, the ability for blood to clot is diminished. The anti-clotting drugs, such as warfarin, coumadin, heparin, etc. work in different ways to interfere with vitamin K, and its role in the clotting process.
I began to understand why medicine uses these drugs after reading Dr. Levy's STOP AMERICA'S #1 KILLER. Some plaques are unstable and the risk of MI is high. His explanation of advanced, aged, unstable plaques reminds one of the growth of ordinary tissue. These plaques can develop their own set of capillaries. As Levy points out, capillaries are weak blood vessels, so when they grow near the heart, the blood pressures are high and risk of rupture increases. A rupture and the subsequent clotting cascade usually leads to an MI. These vitamin K antagonist drugs would thus serve a purpose in certain cases, i.e., to interfere with blood clotting caused by broken capillaries. So it is hard to argue with the use of these drugs in people with advanced plaques being fed by a system of capillaries. (But this risk has to be balanced against the possibility of bleeding in other areas, e.g. in the brain, or from an accident.)
Then there is the issue of calcification. (It is possible one reason rather weak veins keep bypass patients alive for decades is because the veins are being unintentionally strengthened as they become calcified) from the use of the blood thinners.
I suppose there is a balance, but we do know that either a low intake of vitamin K, or taking those vitamin K antagonist drugs will rapidly increase calcification. There is anecdotal evidence (and some clinical evidence) that the arteries will return to a more normal condition after vitamin K supplementation.
I guess I don't understand the clotting concern w/r to AFIB? (I don't know if the family has gotten a clear picture of what really happened, but they were told the Mr. Till had a collapsed blood vessel, perhaps one of his bypass graphs, limiting blood flow to the heart. We have to assume that this is at least one reason why the heart developed AFIB in his case.)